Characterization of Burn Eschar Pericytes

Abstract

Pericytes are cells that reside adjacent to microvasculature and regulate vascular function. Pericytes gained great interest in the field of wound healing and regenerative medicine due to their multipotential fate and ability to enhance angiogenesis. In burn wounds, scarring and scar contractures are the major pathologic feature and cause loss of mobility. The present study investigated the influence of burn wound environment on pericytes during wound healing. Pericytes isolated from normal skin and tangentially excised burn eschar tissues were analyzed for differences in gene and protein expression using RNA-seq., immunocytochemistry, and ELISA analyses. RNA-seq identified 443 differentially expressed genes between normal- and burn eschar-derived pericytes. Whereas, comparing normal skin pericytes to normal skin fibroblasts identified 1021 distinct genes and comparing burn eschar pericytes to normal skin fibroblasts identified 2449 differential genes. Altogether, forkhead box E1 (FOXE1), a transcription factor, was identified as a unique marker for skin pericytes. Interestingly, FOXE1 levels were significantly elevated in burn eschar pericytes compared to normal. Additionally, burn wound pericytes showed increased expression of profibrotic genes periostin, fibronectin, and endosialin and a gain in contractile function, suggesting a contribution to scarring and fibrosis. Our findings suggest that the burn wound environment promotes pericytes to differentiate into a myofibroblast-like phenotype promoting scar formation and fibrosis.

Autophagy gene Atg7 regulates the development of radiation‐induced skin injury and fibrosis of skin

“…Given that Atg7‐deficient mice died within postnatal day 1, 19 we considered using the conditional Atg7 knockout model for the current study. Myofibroblasts, as the major source of excessive ECM synthesis under the pathophysiological conditions that characterize fibrosis, are the critical effector cells in the pathological process of radiation fibrosis 20,21 . Therefore, we decided to conditionally knock out Atg7 in myofibroblasts.…”

“…Myofibroblasts, as the major source of excessive ECM synthesis under the pathophysiological conditions that characterize fibrosis, are the critical effector cells in the pathological process of radiation fibrosis. 20,21 Therefore, we decided to conditionally knock out Atg7 in myofibroblasts. In this way, the potential effect of autophagy on the process of radiation fibrosis can be evaluated in a more convincing way.…”

Tilapia Fish Skin Treatment of Third-Degree Skin Burns in Murine Model

“…Periostin was explored in a mouse wound-repair study, where signaling through integrin molecules was shown to promote the proliferation and migration of fibroblasts [59]. Another study detected overexpression of this peptide in the pericytes of burned skin, and its function was related to scar formation and fibrosis [60]. Gelsolin function is related to actin modulation and clearance after tissue injury [61].…”

The pathogenesis and diagnosis of sepsis post burn injury

“…Microorganisms can rapidly colonize the burn wounds due to thermal destruction of the skin barrier. Burn eschar (avascular necrotic tissue) caused by deep partial-thickness and full-thickness burns provides a protein-rich niche for bacterial colonization and proliferation [ 31 , 32 ]. In addition, burn eschar may also increase the risk of infection by inhibiting early healing via basic fibroblast growth factor-induced endothelial cell proliferation and sprouting [ 33 ].…”